Evidence map›Paper›PMID 28035930›Full record

ArticleJournal of Alzheimer's disease : JAD2017

Investigations into Retinal Pathology in the Early Stages of a Mouse Model of Alzheimer's Disease.

Glyn Chidlow, John P M Wood, Jim Manavis, John Finnie, Robert J Casson

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of Alzheimer's disease : JAD, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.4field-weighted citation impact, top 18% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

27 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Article
  3. Potential Retinal Biomarkers in Alzheimer's Disease.International journal of molecular sciences · 2023
    Review
  4. Article
  5. Article
  6. Acrolein Induces Retinal Abnormalities of Alzheimer's Disease in Mice.International journal of molecular sciences · 2023
    Article
  7. Article
  8. Article
  9. Review
  10. Microglia: Key Players in Retinal Ageing and Neurodegeneration.Frontiers in cellular neuroscience · 2022
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Is the eye a window to the brain in Sanfilippo syndrome?Acta neuropathologica communications · 2020
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 1 country.

Glyn ChidlowOphthalmic Research Laboratories, Hanson Institute Centre for Neurological Diseases, Adelaide, SA, Australia.
John P M WoodOphthalmic Research Laboratories, Hanson Institute Centre for Neurological Diseases, Adelaide, SA, Australia.
Jim ManavisSchool of Medicine, University of Adelaide, Adelaide, SA, Australia.
John FinnieSchool of Medicine, University of Adelaide, Adelaide, SA, Australia.
Robert J CassonOphthalmic Research Laboratories, Hanson Institute Centre for Neurological Diseases, Adelaide, SA, Australia.
Hanson Institute · AUSouth Australia Pathology · AUThe University of Adelaide · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

There is increasing recognition that visual performance is impaired in early stages of Alzheimer's disease (AD); however, no consensus exists as to the mechanisms underlying this visual dysfunction, in particular regarding the timing, nature, and extent of retinal versus cortical pathology. If retinal pathology presents sufficiently early, it offers great potential as a source of novel biomarkers for disease diagnosis. The current project utilized an array of immunochemical and molecular tools to perform a characterization of retinal pathology in the early stages of disease progression using a well-validated mouse model of AD (APPSWE/PS1ΔE9). Analytical endpoints included examination of aberrant amyloid and tau in the retina, quantification of any neuronal degeneration, delineation of cellular stress responses of neurons and particularly glial cells, and investigation of oxidative stress. Brain, eyes, and optic nerves were taken from transgenic and wild-type mice of 3 to 12 months of age and processed for immunohistochemistry, qPCR, or western immunoblotting. The results revealed robust expression of the human APP transgene in the retinas of transgenic mice, but a lack of identifiable retinal pathology during the period when amyloid deposits were dramatically escalating in the brain. We were unable to demonstrate the presence of amyloid plaques, dystrophic neurites, neuronal loss, macro- or micro-gliosis, aberrant cell cycle re-entry, oxidative stress, tau hyperphosphorylation, or upregulations of proinflammatory cytokines or stress signaling molecules in the retina. The overall results do not support the hypothesis that detectable retinal pathology occurs concurrently with escalating amyloid deposition in the brains of APPSWE/PS1ΔE9 mice.

Indexed as

Alzheimer DiseaseAmyloid beta-Protein PrecursorAnimalsBlotting, WesternBrainDisease Models, AnimalDisease ProgressionHumansImmunohistochemistryIn Situ Nick-End LabelingMice, TransgenicNeurogliaNeuronsOptic NerveOrgan SizePlaque, AmyloidAmyloid beta-Protein PrecursorAPP protein, humanMapt protein, mousePresenilin-1PSEN1 protein, humantau ProteinsAlzheimer’s diseaseearly biomarkermicrogliamüller cellretinaretinal ganglion cell

Identifiers

PMID28035930
PMCPMC5271427
OpenAlexW2563150712

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.